The goals of the proposed research are to examine the effects of previously demonstrated changes in diaphragmatic energy metabolism on diaphragmatic contractility. To this end, we will use bilateral phrenic nerve pacing and an inspiratory resistive load to increase diaphragmatic energy expenditure. Stable levels of hypercapnic acidosis and hypoxemia will be induced by administration of 5 percent CO2 in 14 percent O2. Diaphragmatic blood flow and oxygen consumption will be determined at 15, 60 and 120 minutes of bilateral pacing, resistive loading, hypoxia and acidosis. Diaphragmatic contractility will be assessed from measurement of transdiaphragmatic pressure at the stimulating frequency (40 H3) as well as at 20 H3 and 60 H3. One third of the animals will be sacrificed after 15, 60 and 120 minutes respectively, of pacing, resistive loading, hypoxia and acidosis. Analysis of diaphragm metabolites ATP, phosphoryl creatine, lactate and glycogen will make it possible to determine the time course of the metabolic changes, as well as the relation between alterations in diaphragm muscle energy metabolism and contractility. In a second protocol we will employ the same experimental perturbations with one addition. In order to test the effect of diaphragm muscle length on diaphragm endurance and metabolism, we will increase thoracic gas volume by placing the animal's body in a negative pressure box sufficient to increase the resting FRC by 50 percent. In this experiment we will test the hypothesis that working at muscle lengths substantially below the optimum resting length reduces not only the strength of contraction, but also endurance for sustained efforts.